24. Visual disturbance/impairment Flashcards
Gradual painless vision loss:
a) 5 main causes (DRACO)
b) 2 genetic causes
c) Drug causes
d) Neurological causes
e) Environmental causes
* f) Painful causes
a) DRACO:
- Diabetic retinopathy
- Refractive error: improves on pinhole testing
- AMD: central vision loss, distortion of straight lines
- Cataracts: glare in the dark; colours appear dull
- Open-angle glaucoma (chronic): peripheral vision loss
b) - Retinitis pigmentosa: impaired night vision and progressive peripheral vision loss
- Retinal dystrophies: gradual loss of acuity, colour vision
c) Amiodarone (corneal deposits), ethambutol (optic neuritis), hydroxychloroquine (maculopathy), systemic steroids (glaucoma, cataracts)
d) - ON compression (eg. SOL): unilateral vision loss
- Optic chiasm compression: bitemporal hemianopia
- Papilloedema
- TIA/stroke (usually present acutely)
e) Smoking, alcohol, nutritional (vitamin A deficiency - night blindness)
f) Generally indicate more serious pathology (neoplastic or inflammatory):
- Choroidal melanoma, chorioretinitis
- Optic neuritis, sarcoidosis
- SOL
Age-related macular degeneration (AMD).
a) Risk factors
b) Clinical features
c) 2 types
d) Investigations and findings
e) What test is mandatory for diagnosis?
f) Referral for suspected AMD
g) Management of wet AMD
h) Management of dry AMD
a) Age (>55), CVD, FHx, smoking,
b) Central vision loss (may have central scotoma: grey or black patch in central visual field)
- Distortion of straight lines
- Dry is gradual; Wet AMD may be acute onset
c) Wet (10%, treatable) and dry (90%, untreatable);
note - dry AMD can convert to wet AMD
d) - Visual acuity - central vision impaired
- Amsler grid (distortion of straight lines)
- Fundoscopy/ Slit-lamp: drusen (yellow deposits), hyper/hypo-pigmentation of retina; wet - red patches (neovascularisation and bleeding)
- Fluorescein angiography (for diagnosing wet AMD)
e) Ocular coherence tomography
f) Within 1 week (because if wet, treatment could preserve vision)
g) - Anti-VEGF drugs (e.g. ranibizumab, bevacizumab): given as an intra-vitreal injection monthly for 3 months, then variably
h) - Lifestyle advice: smoking cessation, alcohol reduction, healthy balanced diet
- Eye test to see if fit for driving; if not, contact DVLA
- Treat other ocular disease (eg. cataracts, refractive error) and systemic diseases
- Vitamin supplementation for intermediate/ advanced AMD: vitamin C, E, zinc, copper
- Visual rehabilitation
Cataracts.
a) Clinical features - symptom and signs
b) Risk factors
c) Management and risks
a) Gradual reduced vision, faded colours, glare at night (may struggle to drive at night), halos
- Signs: abnormal red reflex,
b) Age, female, smoking, diabetes, systemic steroids/ prolonged topical steroid use, Down syndrome, Marfarn’s, myotonic dystrophy
c) Cataract surgery - phacoemulsification
- Main risk (1 - 3%) is posterior capsule rupture (may rarely cause endophthalmitis - 0.01%)
Chronic open-angle glaucoma.
a) Pathogenesis
b) Cause/risk factors
c) Presentation
d) Investigations
e) Management
a) Optic nerve damage, either by increased IOP (> 21) or normal IOP with increased susceptibility to damage. There is reduced absorption of aqueous humour in the trabecular network
b) FHx, Afro-Caribbean, myopic, HTN, DM
c) Most asymptomatic; progressive and painless gradual peripheral vision loss (then central)
d) - Visual acuity and fields testing
- Goniometry (measure angle between iris and cornea to assess for open/closed angle)
- Tonometry (increased intraocular pressure: >21)
- Slit lamp (increased optic cup:disk ratio)
e) 1st line.
- Prostaglandin analogue (eg. latanoprost): increase aqueous outflow; SE: increased eyelash length
- Beta-BLOCKers (eg. timolol): BLOCK aqueous production (beware asthmatics, heart block)
2nd line.
- combine PG/BB
- add carbonic anhydrase inhibitor (acetazolamide) or miotic (pilocarpine)
3rd line. - laser therapy or surgery
Retinal detachment.
a) What is it?
b) Risk factors
c) Clinical features (3 Fs)
- presentation in infants
d) Examination, investigations and findings
e) Management
f) Prognosis for ‘macula on’ vs. ‘macula off’ RD
g) Main differential of sudden onset flashers/floaters
a) The neurosensory layer of the retina separating off from the underlying retinal pigment epithelium (RPE); often preceded by posterior vitreous detachment (rhegmatogenous RD) - risk is increased further if vitreous haemorrhage (shower of floaters, uncountable)
b) Increasing age, previous Hx of RD (in other eye), lattice degeneration, trauma (eg. paintballing), myopia (longer, thinner eyeball), FHx, Marfan’s, wet AMD
- Exudative RD: inflammatory conditions
c) Sudden onset of unilateral: flashes, floaters, field loss (begins peripherally, moves centrally, curtain-like)
- Infants: white pupillary reflex (leukocoria) or squint (strabismus)
d) - Red reflex - may be abnormal
- RAPD - may be present if macula involved
- Acuity - may be impaired if macula involved
- Fields - loss corresponding to area of detachment
- Slit-lamp/fundoscopy: vitreous opacities/haemorrhages, or detached retinal folds
- OCT
e) - Same day urgent assessment
- Surgical repair: cryotherapy, laser, etc.
f) - Macula-on: can prevent severe vision loss if operated on urgently
- Macula-off: poorer prognosis, can prevent the spread of RD but visual acuity may remain poor post-repair
g) Posterior vitreous detachment - common as you get older, normally benign
Diabetic retinopathy.
a) Clinical features
b) Risk factors
c) Stages of DR and findings on slit-lamp (R0 - R3)
d) Gold standard for diagnosis
e) Management
f) Diabetics at risk of what other eye conditions
a) May be asymptomatic; Chronic vision loss, may start centrally (macular)
b) Duration and severity of hyperglycaemia, nephropathy, hypertension, CVD
c) - No retinopathy (R0): continue with annual screening
- Background DR (R1): microaneurysms and retinal haemorrhages +/- exudates
- Pre-proliferative DR (R2): venous beading, venous loops, dot and blot haemorrhages, cotton wool spots
- Proliferative DR (R3): neovascularisation on the disc (NVD) or elsewhere (NVE), with pre-retinal/vitreous haemorrhages, pre-retinal fibrosis +/- retinal detachment
d) Dilated retinal photography
- may also do OCT, FA
e) - R0/R1: annual review and conservative management; glycaemic control, control of CV risk factors, treat any cataracts, etc.
- R2: Routine ophthalmology review (2 months)
- R3: Fast-tracked ophthalmology review;
Laser therapy, anti-VEGF (for neovascularisation), intra-vitreal steroids (for oedema)
f) - Cataracts (due to excess glucose interfering with the metabolism of the crystalline lens);
- Central retinal vein/artery occlusion
- Hypertensive retinopathy
Sudden loss of vision: differentials.
a) Sudden painless unilateral loss of vision. Cherry red spot on slit lamp
b) Widespread haemorrhages and swollen optic disc
c) Pale and swollen optic disc; headache, scalp tenderness
d) Flashers and floaters; curtain coming down over visual field. Signs?
e) Sudden unilateral vision loss, followed by sudden return of vision
a) Central retinal artery occlusion (Cherry red = artery)
b) Central retinal vein occlusion (lots of back-up of blood with swelling)
c) GCA: requires urgent IV methylprednisolone
d) Retinal detachment: requires urgent surgical re-attachment
e) TIA (may also be impending acute angle-closure glaucoma)
Gradual loss of vision: assessment
- Visual acuity with Snellen Chart
- improve on pinhole? - refractive error/ cataract - Red reflex:
- abnormal? - suggests lens/ corneal/ vitreous pathology (eg. cataracts) - if cataract, opacity does not move; in vitreous/corneal pathology, moves with light direction
- normal? - suggests macular/optic nerve pathology - Visual fields, pupils, colour vision
- Fundoscopy
- Secondary care investigations
Diplopia algorithm.
a) Monocular diplopia - possible diagnoses?
b) Horizontal binocular diplopia (only present with both eyes open)
c) Vertical binocular diplopia
a) Cataract (disappears on pinhole test); Cortical abnormality
b) CN VI palsy (eyes converge when looking to worse side)/ internuclear ophthalmoplegia (eyes diverge when looking to worse side)
c) CN III palsy (ptosis, mydriasis); CN IV palsy; thyroid eye disease
Angle-closure glaucoma.
a) Pathogenesis
b) Risk factors
c) Clinical features
d) Examination, investigations and findings
e) Management
a) Reduced irido-corneal (anterior chamber) angle, causing severely increased IOP due to inability of aqueous humour drainage; usually presents acutely but can have subacute and chronic presentation
b) Short eyeball (severe hypermetropia), increasing age, female, FHx, Marfan’s
c) Sudden onset of ocular pain +/- headache, visual acuity loss, red eye, haloes around light.
- Nausea/vomiting common
d) - Acuity - loss
- Pupils - mid-dilated pupil, non-reactive
- Palpation of globe - stony, hard (indicate high IOP)
- Slit-lamp: shallow anterior chambers in both eyes, closed iridocorneal angle and corneal epithelial oedema
e) - Urgent ophthalmology assessment
- In the meantime, all glaucoma topical medications given: timolol, latanoprost, prednisolone, pilocarpine.
- Also, IV acetazolamide
- Lay patient supine
- Analgesia + antiemetics
- If no effect - IV mannitol
- May require surgery - iridotomy
Acute vision loss: categorising
a) Unilateral, painful
b) Unilateral, painless
c) Bilateral, painful
d) Bilateral, painless
a) Trauma, infection/inflammation (orbital cellulitis, anterior uveitis, ON, endophthalmitis), AACG, contact lens, exposure keratopathy
b) Vascular (CRVO, CRAO, GCA), wet AMD, retinal detachment, vitreous detachment/haemorrhage
c) Arc eye (welders), papilloedema, severe hypertension
d) TIA/stroke, papilloedema
Ocular manifestations of systemic disease.
a) Thyroid eye disease (usually Graves) - features
b) Hyperlipidaemia
c) Systemic steroid use/ prolonged topical steroids
d) Connective tissue disease
e) Causes of dry eye
f) Myasthenia gravis
g) Marfan’s
a) Proptosis (exophthalmos), periorbital oedema, chemosis, red/watery eyes, red/swollen eyelids
b) Corneal arcus; xanthelasma
c) Cataracts, glaucoma, ?infection
d) Anterior uveitis, scleritis, episcleritis
e) Sjogren’s, RA, exposure keratopathy (Bells’ palsy, thyroid eye disease)
f) Asymmetric external ophthalmoplegia, ptosis, weak eye closure, inability to maintain upward gaze, lid lag
g) Lens dislocation, myopia, retinal detachment; irido-corneal angle issue (increased glaucoma risk)
Stages of hypertensive retinopathy.
- Grade 0: No changes
- Grade 1: Mild arterial narrowing (silver wiring)
- Grade 2: Obvious arterial narrowing with focal irregularities (nipping)
- Grade 3: plus… haemorrhages, exudates, cotton wool spots, or retinal oedema
- Grade 4: plus… papilloedema (+/- macula star)
Central retinal artery occlusion (CRAO).
a) Cause/risk factors
b) Presentation
c) Investigations and findings (important DD to exclude)
d) Management
a) “Ocular stroke” - mostly embolic (eg carotid atheroma, AF, endocarditis), inflammatory (GCA, SLE, other vasculitis), thrombophilic disorders
b) - Sudden unilateral painless vision loss (usually reduced to counting fingers; if more severe, could be ophthalmic artery ischaemia)
c) - Reduced visual acuity
- RAPD
- Fundoscopy: cherry red spot on macula
- ESR if > 60 yrs to rule out GCA as a cause (treatable!)
d) - Urgent ophthalmology review
- Assess for CV disease: pulse (AF), carotid bruits, BP
- If GCA - IV methylprednisolone
- If atherosclerotic cause: massage the orbit (may rarely dislodge the embolus), lower IOP (as for AACG)
- Secondary prevention: statin, asprin, BP etc.
Central retinal vein occlusion (CRVO).
a) Causes and risk factors
b) Clinical features
c) Investigations and findings
d) Management
a) Age, CV risk factors, diabetes, raised IOP, hyperviscosity, thrombophilia
b) Sudden painless unilateral vision loss/blurring, often starts on waking up
c) - Visual acuity reduced
- RAPD may be present
- Fundoscopy: widespread flame haemorrhages, macular oedema, neovascularisation
d) - Urgent ophthalmology review
- Reduce IOP
- Anti-VEGF
- Address any underlying modifiable risk factors
